The hyposerotonergic hypothesis of adolescent depression (MDD) is examined via 3 pathways: 1)low dose (12.5 mg) IV clomiproamine (CMI) as a serotonergic probe in adolescent MDD compared to matched controls; 2) indexing of the serotonin transporter in depressives vs controls as a potential marker, and assessment pre and post treatment with an SRI as a potential trial marker of MDD in this population; 3) use of high dose (200mg) pulse IV CMI (an SRI when given IV) to determine acute efficacy in adolescent MDD.